Is Urinary Prostaglandin E2 Excretion Correlated to Urinary Excretion of Calcium, Sodium and Potassium?

Author(s):  
M. Hegemann ◽  
M. Weitbrecht ◽  
I. B�ttger ◽  
S. Nigam ◽  
R. Pfab
PEDIATRICS ◽  
1958 ◽  
Vol 22 (4) ◽  
pp. 773-773

Recently considerable interest has been directed at the comparative rates of utilization of glucose and fructose, administered intravenously. The present study was designed to carry out such a comparison using intakes of the carbohydrates which would provide sufficient calories to meet the maintenance requirements. The observations included a comparison of the extent of accumulation of certain acid metabolites and disturbances of the acid-base equilibrium which result from the rapid infusion of glucose and fructose. It was found that infusions of glucose and fructose in solution with electrolytes at 1 gm/kg/hr enabled both sugars to be utilized completely, without significant differences in the excretion of water, sodium and potassium. When the sugars were infused at a rate of 2 gm/kg/hr, 20% of the glucose and 9.9% of the fructose were excreted in the urine. Excretion of sodium in the urine with infusions of glucose led to loss of 79% of the intake, while for fructose the urinary excretion was 127% of intake, although no significant differences in excretion of water and potassium were noted. Infusions of fructose were accompanied by much greater increases of lactate and pyruvate in the blood than were caused by infusions of glucose. The urinary excretion of lactic acid was also greater with fructose than with glucose. It is stated that the superior utilization of fructose at rapid rates of infusion is not entirely advantageous because of the accompanying acidosis, which is of sufficient severity to make limitation of the rate of its infusion advisable.


Hypertension ◽  
2014 ◽  
Vol 63 (2) ◽  
pp. 238-244 ◽  
Author(s):  
Ying Huang ◽  
Linda Van Horn ◽  
Lesley F. Tinker ◽  
Marian L. Neuhouser ◽  
Laura Carbone ◽  
...  

1981 ◽  
Vol 7 (4) ◽  
pp. 261-266 ◽  
Author(s):  
M. Blum ◽  
A. Algueti ◽  
S. Bauminger ◽  
A. Aviram ◽  
D. Ayalon

Nutrients ◽  
2016 ◽  
Vol 8 (4) ◽  
pp. 191 ◽  
Author(s):  
Carrie Service ◽  
Carley Grimes ◽  
Lynn Riddell ◽  
Feng He ◽  
Karen Campbell ◽  
...  

BMJ ◽  
2019 ◽  
pp. l772 ◽  
Author(s):  
Martin O’Donnell ◽  
Andrew Mente ◽  
Sumathy Rangarajan ◽  
Matthew J McQueen ◽  
Neil O’Leary ◽  
...  

AbstractObjectiveTo evaluate the joint association of sodium and potassium urinary excretion (as surrogate measures of intake) with cardiovascular events and mortality, in the context of current World Health Organization recommendations for daily intake (<2.0 g sodium, >3.5 g potassium) in adults.DesignInternational prospective cohort study.Setting18 high, middle, and low income countries, sampled from urban and rural communities.Participants103 570 people who provided morning fasting urine samples.Main outcome measuresAssociation of estimated 24 hour urinary sodium and potassium excretion (surrogates for intake) with all cause mortality and major cardiovascular events, using multivariable Cox regression. A six category variable for joint sodium and potassium was generated: sodium excretion (low (<3 g/day), moderate (3-5 g/day), and high (>5 g/day) sodium intakes) by potassium excretion (greater/equal or less than median 2.1 g/day).ResultsMean estimated sodium and potassium urinary excretion were 4.93 g/day and 2.12 g/day, respectively. After a median follow-up of 8.2 years, 7884 (6.1%) participants had died or experienced a major cardiovascular event. Increasing urinary sodium excretion was positively associated with increasing potassium excretion (unadjusted r=0.34), and only 0.002% had a concomitant urinary excretion of <2.0 g/day of sodium and >3.5 g/day of potassium. A J-shaped association was observed of sodium excretion and inverse association of potassium excretion with death and cardiovascular events. For joint sodium and potassium excretion categories, the lowest risk of death and cardiovascular events occurred in the group with moderate sodium excretion (3-5 g/day) and higher potassium excretion (21.9% of cohort). Compared with this reference group, the combinations of low potassium with low sodium excretion (hazard ratio 1.23, 1.11 to 1.37; 7.4% of cohort) and low potassium with high sodium excretion (1.21, 1.11 to 1.32; 13.8% of cohort) were associated with the highest risk, followed by low sodium excretion (1.19, 1.02 to 1.38; 3.3% of cohort) and high sodium excretion (1.10, 1.02 to 1.18; 29.6% of cohort) among those with potassium excretion greater than the median. Higher potassium excretion attenuated the increased cardiovascular risk associated with high sodium excretion (P for interaction=0.007).ConclusionsThese findings suggest that the simultaneous target of low sodium intake (<2 g/day) with high potassium intake (>3.5 g/day) is extremely uncommon. Combined moderate sodium intake (3-5 g/day) with high potassium intake is associated with the lowest risk of mortality and cardiovascular events.


1984 ◽  
Vol 246 (2) ◽  
pp. F201-F204 ◽  
Author(s):  
J. D. Horisberger ◽  
J. Diezi

The effects of actinomycin D on short-term response to aldosterone on sodium and potassium urinary excretion were investigated in adrenalectomized glucocorticoid-substituted anesthetized rats. Aldosterone alone (1 microgram/kg followed by sustained intravenous infusion of 1 microgram X kg-1 X h-1) entailed a simultaneous antinatriuretic and kaliuretic effect after a latent period of 30-60 min. Actinomycin D (300 micrograms/kg) administered intravenously 30 min before aldosterone inhibited both the aldosterone-induced kaliuresis and antinatriuresis and the concomitant changes in plasma potassium concentration. The administration of actinomycin D alone enhanced sodium excretion in the first hour and then induced kaliuresis. These results favor the hypothesis that mineralocorticoid effects of aldosterone on sodium and potassium excretion are closely linked and may be dependent on the same mechanisms.


1992 ◽  
Vol 83 (1) ◽  
pp. 75-80 ◽  
Author(s):  
C. Henríquez-la Roche ◽  
B. Rodríguez-Iturbe ◽  
G. Parra

1. Urinary excretion of prostaglandin E2 is increased in patients with idiopathic hypercalciuria, but in order to conclude that hyperprostaglandinuria is a primary phenomenon, it must be demonstrated that high levels of urinary prostaglandin E2 can be dissociated from other factors, such as urine volume and natriuresis, and from the hypercalciuria itself. 2. We studied 10 patients with idiopathic hypercalciuria and 10 control subjects on high and low calcium diets providing daily calcium intakes of 30-35 mmol and 7.5-10 mmol, respectively, and similar sodium intakes. In addition, patients with idiopathic hypercalciuria and control subjects were studied during water restriction and water diuresis. 3. Urinary prostaglandin E2 excretion was more than twice as high in patients with idiopathic hypercalciuria than in control subjects on the low and high calcium diets as well as during water restriction and water diuresis (P<0.01). 4. Urinary prostaglandin E2 excretion was not affected by changes in urinary calcium excretion in patients with idiopathic hypercalciuria and in control subjects. Patients with idiopathic hypercalciuria on the low calcium diet and control subjects on the high calcium diet had similar levels of calciuria and natriuresis, yet urinary prostaglandin E2 excretion (mean ± SEM) was 11.62 ± 1.71 nmol/day in the patients with idiopathic hypercalciuria and 3.26 ± 0.48 nmol/day in the control subjects (P= 0.0006). 5. These results indicate that increased urinary prostaglandin E2 excretion is a cardinal characteristic of patients with idiopathic hypercalciuria.


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